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1 bitor, and a component of LCZ696 (sacubitril/valsartan).
2 tions among patients treated with sacubitril-valsartan.
3 reatment with enalapril than with sacubitril/valsartan.
4  weeks (14% reduction; P=0.03) compared with valsartan.
5 kers of heart failure severity compared with valsartan.
6 hese genes was preserved by naloxone but not valsartan.
7 ting the angiotensin II type I receptor with valsartan.
8 ion, a failure prevented by naloxone but not valsartan.
9 as relevant in a decision aid for sacubitril/valsartan.
10 d slowed decline in eGFR, in comparison with valsartan.
11  before and during treatment with sacubitril/valsartan.
12 ngfully early after initiation of sacubitril/valsartan.
13 n who derive greater benefit from sacubitril/valsartan.
14 on were initiated and titrated on sacubitril/valsartan.
15 during the first 8 to 10 weeks of sacubitril/valsartan.
16 angiotensin receptor blockers, or sacubitril-valsartan.
17 1012], 12 weeks, 835 [710-981]; ratio LCZ696/valsartan, 0.77, 95% CI 0.64-0.92, p=0.005).
18 s 29% lower in patients receiving sacubitril/valsartan (114 [7%] patients) compared with patients rec
19  were randomly assigned to LCZ696 and 152 to valsartan; 134 in the LCZ696 group and 132 in the valsar
20 (455), a combination of aliskiren 150 mg and valsartan 160 mg (446), or placebo (459) for 4 weeks, fo
21 receive once-daily aliskiren 150 mg (n=437), valsartan 160 mg (455), a combination of aliskiren 150 m
22 led trial of angiotensin II receptor blocker valsartan 160 mg twice daily compared with placebo in pa
23 odialysis to placebo, ramipril (5 mg/d), and valsartan (160 mg/d) for 7 days, with a washout period o
24 6 patients were randomly assigned to receive valsartan; 198 were randomly assigned to receive placebo
25 R was less for sacubitril/valsartan than for valsartan (-2.0 [95% CI, -2.2 to -1.9] versus -2.7 [95%
26 ted with adverse effects similar to those of valsartan; 22 patients (15%) on LCZ696 and 30 (20%) on v
27 mly assigned to enalapril than to sacubitril/valsartan (3.1 vs 2.2 per 100 patient-years; HR, 1.37 [9
28 han to those randomly assigned to sacubitril/valsartan (3.3 vs 2.3 per 100 patient-years; HR, 1.43 [9
29 int, the combination of aliskiren 300 mg and valsartan 320 mg lowered mean sitting diastolic blood pr
30 iskiren 300 mg 9.0 mm Hg decrease, p<0.0001; valsartan 320 mg, 9.7 mm Hg decrease, p<0.0001), or with
31 1.2 mm Hg, 95% CI -2.3 to -0.1; p=0.030) and valsartan 320 mg/day (-4.4 mm Hg, -5.4 to -3.3; p<0.0001
32 dy physician to polypill two, which included valsartan 40 mg instead of enalapril 5 mg.
33 eated animals with animals treated with oral valsartan (50 mg/kg/d), oral enalapril (10 mg/kg/d), and
34  mg/day), nebivolol (5 mg/day or 20 mg/day), valsartan (80 mg/day or 160 mg/day), or placebo.
35 th enalapril 10 mg twice daily or sacubitril/valsartan 97/103 mg twice daily (previously known as LCZ
36 (LVEF) </=40%] were randomized to sacubitril/valsartan 97/103 mg twice daily versus enalapril 10 mg t
37                                   Sacubitril/valsartan, a combination angiotensin receptor-neprilysin
38                                Compared with valsartan, absolute risk reductions with sacubitril/vals
39 hether the BP-lowering effects of sacubitril/valsartan accounted for its treatment effects.
40                Notable were the formation of valsartan acid from irbesartan and valsartan, the persis
41  transformation products metoprolol acid and valsartan acid were formed along the reach under all con
42 and assessed the effectiveness of sacubitril/valsartan across the LVEF spectrum.
43                                   Sacubitril/valsartan across the spectrum of ejection fraction in he
44                            Most importantly, valsartan administration also attenuated the development
45                         Neither ramipril nor valsartan affected BP during hemodialysis.
46 % (95% CI: 1% to 8%; p = 0.02) compared with valsartan alone, consistently in men and women and patie
47                                         With valsartan alone, the rate of total primary events was 26
48 ltered by sacubitril/valsartan compared with valsartan alone.
49 these biomarkers were compared with those of valsartan alone.
50 y profile similar to that with aliskiren and valsartan alone.
51 ion, 440 were assigned to receive sacubitril-valsartan and 441 to receive enalapril.
52 in 33 patients (1.4%) assigned to sacubitril/valsartan and 64 patients (2.7%) assigned to valsartan (
53 or the syntheses of industrial precursors to valsartan and boscalid from chloroarenes with approximat
54                      The interaction between valsartan and CKD was also tested.
55 rsus 17% of patients treated with sacubitril/valsartan and enalapril, respectively.
56 he wholesale acquisition cost for sacubitril/valsartan and enalapril.
57 index date was the first fill for sacubitril/valsartan and if none, for an ACEI or ARB.
58    Small but significant differences between valsartan and placebo were present for change in right v
59                                              Valsartan and ramipril both lowered D-dimer levels (P<0.
60                                              Valsartan and ramipril both lowered IL-6 levels during d
61                                         Both valsartan and tempol substantially attenuated mitochondr
62 tensin type 1 receptor blockers losartan and valsartan and the angiotensin-converting enzyme inhibito
63 rtan+LBQ augmented the inhibitory effects of valsartan and the highest doses completely abrogated ang
64 o) combines the angiotensin receptor blocker valsartan and the neprilysin inhibitor prodrug sacubitri
65           The association between sacubitril/valsartan and the primary outcome was not modified by ba
66  dysfunction vs. vehicle and both sacubitril/valsartan and valsartan attenuated progressive LV dilati
67               After 5 weeks, both sacubitril/valsartan and valsartan reduced CTGF expression in the r
68               In the border zone, sacubitril/valsartan and valsartan reduced hypertrophic markers, bu
69        Rates of adverse events for losartan, valsartan, and candesartan users (N=136 177) aged >/=66
70             Among generic users of losartan, valsartan, and candesartan, there was an increase in rat
71 on fraction, favorably altered by sacubitril/valsartan, and have important prognostic value.
72  on target doses of beta-blocker, sacubitril/valsartan, and mineralocorticoid receptor antagonists.
73 d 1.26 +/- 0.10 for no treatment, enalapril, valsartan, and SK-1080, respectively).
74 ot modify the treatment effect of sacubitril/valsartan, and the BP-lowering effects of sacubitril/val
75        We compared the effects of captopril, valsartan, and their combination on atherosclerotic even
76 s effect was proposed after results from the Valsartan Antihypertensive Long-Term Use Evaluation (VAL
77 valuation (VALUE) trial, in which the use of valsartan (ARB) was compared with amlodipine in patients
78 found an excess of MIs among patients in the valsartan arm.
79 ith vehicle (water), sacubitril/valsartan or valsartan, as comparator group, for either 1 or 5 weeks.
80 duced NT-proBNP to a greater extent than did valsartan at 12 weeks and was well tolerated.
81 nfidence interval: 4.4 to 6.0) compared with valsartan at 4 weeks, which was not modified by baseline
82             The combination of aliskiren and valsartan at maximum recommended doses provides signific
83 s. vehicle and both sacubitril/valsartan and valsartan attenuated progressive LV dilation after 1 and
84  CI 670-914], 12 weeks, 605 pg/mL [512-714]; valsartan: baseline, 862 pg/mL [733-1012], 12 weeks, 835
85 ibitory effects of the clinical AT1R blocker valsartan can be identified, whereas blockage of upstrea
86 trophic cardiomyopathy (HCM) to test whether valsartan can modify disease progression.
87                                              Valsartan can slow progression and/or reverse early card
88                                              Valsartan, captopril, or the combination had comparable
89  randomly assigned to receive treatment with valsartan, captopril, or the combination; follow-up cont
90                    Treatment with sacubitril/valsartan caused a rightward shift in the distribution o
91                       Conversely, sacubitril/valsartan, combining NP degradation inhibition through n
92 trated consistent improvements in sacubitril/valsartan compared with enalapril through 36 months.
93 comes and on the effectiveness of sacubitril/valsartan compared with enalapril.
94 e better in patients treated with sacubitril/valsartan compared with those treated with enalapril, wi
95 matrix homeostasis are altered by sacubitril/valsartan compared with valsartan alone.
96 relative and absolute benefits of sacubitril/valsartan compared with valsartan in HFpEF appear to be
97            The benefit of LCZ696 (sacubitril/valsartan) compared with enalapril was consistent across
98 e maximum recommended doses of aliskiren and valsartan, compared with each drug alone in patients wit
99           Treatment of HFrEF with sacubitril-valsartan, compared with enalapril, did not significantl
100 ixteen weeks after randomization, sacubitril/valsartan decreased tissue inhibitor of matrix metallopr
101 n, and the BP-lowering effects of sacubitril/valsartan did not account for its effects on outcomes, r
102         Moreover, high dietary potassium and valsartan each augmented the inhibitory effect of 11,12-
103 s, a high potassium intake or treatment with valsartan enhanced AA-induced inhibition of ENaC, an eff
104 of double-blind treatment with nebivolol and valsartan fixed-dose combination (5 and 80 mg/day, 5 and
105                                Nebivolol and valsartan fixed-dose combination is an effective and wel
106                                   Sacubitril/valsartan for 1-week limited LV contractile dysfunction
107                            The VANISH trial (Valsartan for Attenuating Disease Evolution in Early Sar
108 hydrochlorothiazide, and either enalapril or valsartan for primary and secondary prevention of cardio
109  reduction in primary events with sacubitril/valsartan from patients hospitalized within 30 days (rat
110                        The application of 1% valsartan gel compared with other tested formulations an
111                               One percent of valsartan gel-treated wounds also exhibited higher mitoc
112  group and 0.26% (SD 1.25) in the sacubitril/valsartan group (between-group reduction 0.13%, 95% CI 0
113  weeks in the LCZ696 group compared with the valsartan group (LCZ696: baseline, 783 pg/mL [95% CI 670
114 d by 0.60 (SD 1.4) cm/s from baseline in the valsartan group (p<0.0001) and 0.44 (1.4) cm/s from base
115 .9) mm Hg reduction in blood pressure in the valsartan group and a 9.7 (17.0)/5.5 (10.2) mm Hg reduct
116 23.8 to 218.9 dyne x s/cm5 in the sacubitril-valsartan group and increased from 213.2 to 214.4 dyne x
117 he baseline value was 0.53 in the sacubitril-valsartan group as compared with 0.75 in the enalapril g
118 esults of Base-Case Analysis: The sacubitril-valsartan group experienced 0.08 fewer heart failure hos
119                      At 8 months, sacubitril/valsartan group noted improvements in both KCCQ clinical
120 ns were persistently lower in the sacubitril/valsartan group than in the enalapril group over the 3-y
121  was significantly greater in the sacubitril-valsartan group than in the enalapril group; the ratio o
122 rtan; 134 in the LCZ696 group and 132 in the valsartan group were included in analysis of the primary
123 the valsartan group, and 37 in the aliskiren/valsartan group), mainly due to lack of therapeutic effe
124  group, 53 in the aliskiren group, 43 in the valsartan group, and 37 in the aliskiren/valsartan group
125 gator reported events 798), 587 (796) in the valsartan group, and 554 (756) in the combination group;
126 (0.77, 0.58-1.02, p=0.073) in the sacubitril/valsartan group.
127  g; P=0.01) in the placebo group than in the valsartan group.
128 eased by a similar amount in the placebo and valsartan groups (P=0.94).
129 olled in PARADIGM-HF who received sacubitril/valsartan had a greater long-term reduction in HbA1c tha
130 treated with a beta-blocker or randomized to valsartan had greater odds of being in the HFiEF group,
131                                   Sacubitril/valsartan had more consistent effects than valsartan on
132  22 patients (15%) on LCZ696 and 30 (20%) on valsartan had one or more serious adverse event.
133                                   Sacubitril/valsartan has been approved for use in heart failure (HF
134 valsartan and 64 patients (2.7%) assigned to valsartan (hazard ratio, 0.50 [95% CI, 0.33-0.77]; P=0.0
135  independent randomized clinical trials, the Valsartan Heart Failure Trial (Val-HeFT) (n=4053) and th
136         Of the 5010 subjects enrolled in the Valsartan Heart Failure Trial (Val-HeFT), 3519 had a bas
137 onths (n=1517) in patients randomized in the Valsartan Heart Failure Trial (Val-HeFT).
138 4 months (n=1345), and 12 months (n=1094) in Valsartan Heart Failure Trial.
139                                   Sacubitril/valsartan improved congestion to a greater extent than d
140 ocardial infarction who were enrolled in the Valsartan in Acute Myocardial Infarction (VALIANT) echoc
141 entation for 1067 patients who had SD in the Valsartan in Acute Myocardial Infarction Trial (VALIANT)
142  as sudden death events in patients from the VALsartan In Acute myocardial infarctioN Trial (VALIANT)
143  events in 14,703 patients randomized in the Valsartan in Acute Myocardial Infarction Trial (VALIANT)
144                                 The VALIANT (Valsartan in Acute Myocardial Infarction Trial) Echo stu
145 0 African-American patients) in the VALIANT (VALsartan In Acute myocardial iNfarcTion) trial were com
146 , and degradation, are altered by sacubitril/valsartan in comparison to enalapril.
147 patients with HFrEF is reduced by sacubitril/valsartan in comparison with enalapril.
148                           METHODS AND In the Valsartan in Heart Failure Trial (Val-HeFT), 5010 patien
149 nefits of sacubitril/valsartan compared with valsartan in HFpEF appear to be amplified when initiated
150 hanisms underlying the effects of sacubitril-valsartan in HFrEF.
151                           In Nateglinide and Valsartan in Impaired Glucose Tolerance Outcomes Researc
152 e), the in-hospital initiation of sacubitril/valsartan in patients hospitalized for acute decompensat
153                          (LCZ696 Compared to Valsartan in Patients With Chronic Heart Failure and Pre
154 ion) trial tested the efficacy of sacubitril-valsartan in patients with heart failure with preserved
155 ic explanation for the effects of sacubitril-valsartan in patients with HFrEF.
156 f clinical events and response to sacubitril/valsartan in relation to time from last HF hospitalizati
157 s, and 9 months of treatment with sacubitril/valsartan in the PARADIGM-HF (Prospective Comparison of
158 lol) and an angiotensin II receptor blocker (valsartan) in adults with hypertension.
159                                              Valsartan increased F(2)-isoprostane levels, and ramipri
160                   In the infarct, sacubitril/valsartan induced an early uptake of (99m)Tc-NC100692 (a
161             In summary, during hemodialysis, valsartan induces a greater anti-inflammatory effect com
162 tensin receptor blocker component of LCZ696, valsartan inhibited both hypertrophy and fibrosis.
163 for lack of guideline-recommended sacubitril/valsartan initiation warrant investigation and may revea
164        Limitation: The benefit of sacubitril-valsartan is based on a single clinical trial.
165                                         Dual valsartan+LBQ augmented the inhibitory effects of valsar
166 ure (PARADIGM-HF) trial, in which sacubitril/valsartan (LCZ696) reduced both death and HF hospitaliza
167 sin receptor neprilysin inhibitor sacubitril/valsartan (LCZ696) reduced cardiovascular morbidity and
168 ht to determine if treatment with sacubitril/valsartan (LCZ696) reduces rates of hospital readmission
169   These findings demonstrate that sacubitril/valsartan leads to better HRQL in surviving patients wit
170                    Treatment with sacubitril/valsartan led to inconsistent changes in BNP, which vari
171       Initiation and titration of sacubitril/valsartan led to variable changes in concentrations of m
172       These findings suggest that sacubitril/valsartan may reduce profibrotic signaling, which may co
173           These data suggest that sacubitril/valsartan might enhance glycaemic control in patients wi
174 AAF, suggesting that the angiotensin blocker valsartan might prevent HAAF.
175  with initiation and titration of sacubitril/valsartan, more than doubling by the first follow-up vis
176            Randomization (1:1) to sacubitril-valsartan (n = 231; target dosage, 97/103 mg twice daily
177  to receive sacubitril/valsartan (n=2419) or valsartan (n=2403).
178 rved ejection fraction to receive sacubitril/valsartan (n=2419) or valsartan (n=2403).
179                      A total of 88 patients (valsartan, n=44; placebo, n=44) were enrolled in the tri
180                        Effects of sacubitril/valsartan on atrial natriuretic peptide (ANP) concentrat
181 udy was to examine the effects of sacubitril/valsartan on biomarkers of ECM homeostasis and the assoc
182 study investigated the effects of sacubitril/valsartan on biomarkers of extracellular matrix homeosta
183                    The effects of sacubitril/valsartan on biomarkers were compared with enalapril.
184                     The effect of sacubitril-valsartan on cardiac remodeling is uncertain.
185 o assess the treatment effects of sacubitril/valsartan on congestion.
186                                The effect of valsartan on estimated glomerular filtration rate was es
187                     The beneficial effect of valsartan on first morbid events was similar in those wi
188 l/valsartan had more consistent effects than valsartan on LV remodeling in experimental HF.
189                                The effect of valsartan on mortality did not differ in patients with a
190  sacubitril and angiotensin receptor blocker valsartan on myocardial remodeling and cardiac perfusion
191  whether the treatment effects of sacubitril/valsartan on outcomes are related to BP lowering, partic
192  sought to examine the effects of sacubitril/valsartan on results from different natriuretic peptide
193 There was no significant treatment effect of valsartan on right ventricular ejection fraction, exerci
194                    The effects of sacubitril/valsartan on these biomarkers were compared with those o
195 ion, and the effect of LCZ696, compared with valsartan, on hs-TnT over 36 weeks.
196   (Efficacy and Safety of LCZ696 Compared to Valsartan, on Morbidity and Mortality in Heart Failure P
197 ndomly assigned to treatment with sacubitril/valsartan or enalapril.
198 line, 12 and 36 weeks after randomization to valsartan or LCZ696.
199 ine and another combination drug, sacubitril/valsartan or LCZ696.
200      Intervention: Treatment with sacubitril-valsartan or lisinopril.
201 emia, with or without concurrent exposure to valsartan or naloxone.
202 rt failure were randomly assigned to receive valsartan or placebo.
203 improved with either ANG II receptor blocker valsartan or superoxide dismutase/catalase mimetic tempo
204 o treatment with vehicle (water), sacubitril/valsartan or valsartan, as comparator group, for either
205  between Sprague-Dawley, untreated Ren2, and valsartan- or tempol-treated Ren2 rats.
206                    The benefit of sacubitril/valsartan over enalapril was similar to the primary outc
207                    The benefit of sacubitril/valsartan, over an angiotensin-converting enzyme inhibit
208                                              Valsartan prevented CsA-induced oxidative stress as well
209  remote myocardium, although only sacubitril/valsartan prevented interstitial fibrosis.
210        Conclusion: Treatment with sacubitril-valsartan provides reasonable value in reducing cardiova
211 ed hypertrophic markers, but only sacubitril/valsartan reduced cardiomyocyte size and increased VEGFA
212      We further evaluated whether sacubitril/valsartan reduced congestion during follow-up and whethe
213 After 5 weeks, both sacubitril/valsartan and valsartan reduced CTGF expression in the remote myocardi
214                                              Valsartan reduced estimated glomerular filtration rate c
215 In the border zone, sacubitril/valsartan and valsartan reduced hypertrophic markers, but only sacubit
216  and Morbidity in Heart Failure), sacubitril/valsartan reduced morbidity and mortality compared with
217  fraction, whether treatment with sacubitril/valsartan reduced NT-proBNP below specific partition val
218                                   Sacubitril/valsartan reduced SBP by 5.2 mm Hg (95% confidence inter
219                          However, sacubitril/valsartan reduced SBP more in women (6.3 mm Hg) than men
220                                              Valsartan reduced the estimated glomerular filtration ra
221 with preserved ejection fraction, sacubitril/valsartan reduced the risk of renal events, and slowed d
222                                   Sacubitril/valsartan reduced the risk of the primary outcome irresp
223          Compared with enalapril, sacubitril-valsartan reduces cardiovascular mortality and heart fai
224  fraction (HFrEF), treatment with sacubitril-valsartan reduces N-terminal pro-b-type natriuretic pept
225  patients with HFrEF treated with sacubitril-valsartan, reduction in NT-proBNP concentration was weak
226 ril did not reduce focal tracer uptake, oral valsartan resulted in partial blockade (infarct-to-remot
227 trated the efficacy and safety of sacubitril/valsartan (S/V) in stabilized patients with acute decomp
228 ar (LV) ejection fraction <=40%), sacubitril/valsartan (S/V) treatment is associated with improved he
229 blocker and neprilysin inhibitor, sacubitril/valsartan (Sac/Val, LCZ696), will attenuate PH and impro
230 of drugs for the treatment of heart failure: Valsartan/sacubitril (formerly known as LCZ696 and curre
231 g clinical trials are evaluating the role of valsartan/sacubitril in the treatment of heart failure w
232 bidity in Heart Failure (PARADIGM-HF) trial, valsartan/sacubitril significantly reduced mortality and
233  identify a PKG-dependent mechanism by which valsartan/sacubitril, a combination drug recently approv
234   We review here the mechanisms of action of valsartan/sacubitril, the pharmacological properties of
235 hat the in-hospital initiation of sacubitril/valsartan should be routinely considered for patients wi
236                       Compared with placebo, valsartan significantly (P<0.001) reduced the rate of in
237 F with reduced ejection fraction, sacubitril/valsartan significantly decreased many of these biomarke
238 hat preventive treatment of Tg2576 mice with valsartan significantly reduced AD-type neuropathology a
239                                              Valsartan significantly reduced arterial pressure in kno
240                                              Valsartan significantly reduced the RDS after 6 months v
241 up healthcare utilization between sacubitril/valsartan switchers and ACEI or ARB maintainers.
242 were randomly assigned to receive sacubitril-valsartan (target dose, 97 mg of sacubitril with 103 mg
243  PIIINP had decreased more in the sacubitril/valsartan than enalapril group.
244  The decline in eGFR was less for sacubitril/valsartan than for valsartan (-2.0 [95% CI, -2.2 to -1.9
245 ions from baseline were seen with sacubitril-valsartan than with enalapril in all others, including l
246  the NT-proBNP concentration with sacubitril-valsartan than with enalapril was evident as early as we
247 erspectives on a decision aid for sacubitril/valsartan that explicitly addresses out-of-pocket costs.
248 blicly available decision aid for sacubitril/valsartan that explicitly incorporates considerations re
249 mation of valsartan acid from irbesartan and valsartan, the persistence of N-desmethylvenlafaxine acr
250         Whether the initiation of sacubitril-valsartan therapy is safe and effective among patients w
251  heart failure, the initiation of sacubitril-valsartan therapy led to a greater reduction in the NT-p
252    There was no significant effect of 3-year valsartan therapy on systemic right ventricular ejection
253                       Background: Sacubitril-valsartan therapy reduces cardiovascular mortality compa
254 en improvements in mortality with sacubitril/valsartan, this analysis provides comprehensive assessme
255  Given the biochemical targets of sacubitril/valsartan, this study hypothesized that circulating biom
256  to LCZ696 titrated to 200 mg twice daily or valsartan titrated to 160 mg twice daily, and treated fo
257 eive either the angiotensin receptor blocker valsartan (titrated to 320 mg once daily) or matched pla
258 receptor blocker), be switched to sacubitril/valsartan to reduce morbidity and mortality.
259 ical validity of measuring BNP in sacubitril/valsartan-treated patients has been questioned, and use
260                                In sacubitril/valsartan-treated patients, median NT-proBNP was signifi
261 tant insights into the effects of sacubitril/valsartan treatment on individual patient results, and f
262  Results of Sensitivity Analysis: Sacubitril-valsartan treatment was most sensitive to the duration o
263 ental costs and QALYs gained with sacubitril/valsartan treatment were estimated at $35512 and 0.78, r
264                              With sacubitril/valsartan treatment, B-type natriuretic peptide (BNP) co
265 independent of clinical variables, sST2, and valsartan treatment.
266 get dose, 97 mg of sacubitril with 103 mg of valsartan twice daily) or enalapril (target dose, 10 mg
267                                   Sacubitril/valsartan use was associated with a lower risk for all-c
268                It has been demonstrated that Valsartan (Val) as an angiotensin receptor blocker has r
269                   We studied the efficacy of valsartan (Val) to slow cardiovascular disease progressi
270 consists of an angiotensin receptor blocker (valsartan [VAL]) and a neprilysin inhibitor (sacubitril
271 hether the efficacy and safety of sacubitril/valsartan varies in relation to the proximity to hospita
272 questions are the efficacy of the sacubitril/valsartan-vericiguat combination in HFrEF and of vericig
273 valuate the cost-effectiveness of sacubitril-valsartan versus angiotensin-converting enzyme inhibitor
274 oup, and 554 (756) in the combination group; valsartan versus captopril, p = 0.651 (0.965); combinati
275                      Overall, the sacubitril/valsartan versus enalapril hazard ratio for the primary
276                    (Comparison of Sacubitril/Valsartan Versus Enalapril on Effect of NT-proBNP in Pat
277      In PIONEER-HF (Comparison of Sacubitril/Valsartan Versus Enalapril on Effect on NT-pro BNP in Pa
278     The PIONEER-HF (comParIson Of sacubitril/valsartaN versus Enalapril on Effect on nt-pRo-bnp in pa
279 imed to investigate the effect of sacubitril/valsartan versus enalapril on HbA1c and time to first-ti
280 s with HFrEF who were switched to sacubitril/valsartan versus maintained on an ACEI or ARB.
281 rdiovascular risk factors were randomized to valsartan versus placebo and nateglinide versus placebo
282 r ejection fraction (34%-36% with sacubitril-valsartan vs 33 to 35% with enalapril; treatment differe
283 000 patients with HF treated with sacubitril/valsartan vs enalapril over 30 years.
284  vs. -25.3%; ratio of change with sacubitril-valsartan vs. enalapril, 0.71; 95% confidence interval [
285 sin receptor neprilysin inhibitor sacubitril/valsartan was associated with a reduction in cardiovascu
286                                              Valsartan was associated with a similar frequency of sig
287                     The effect of sacubitril/valsartan was consistent across all subgroups examined.
288                                   Sacubitril/valsartan was effective across the LVEF spectrum, with n
289                                   Sacubitril/valsartan was effective at reducing cardiovascular death
290                                   Sacubitril-valsartan was initiated and the dose adjusted.
291 sin receptor neprilysin inhibitor sacubitril/valsartan was more effective than the angiotensin-conver
292                    Treatment with sacubitril/valsartan was nearly twice as likely as enalapril to red
293 we found that only 1 of the candidate drugs, valsartan, was capable of attenuating oligomerization of
294  Given the biochemical targets of sacubitril/valsartan, we hypothesized that circulating biomarkers r
295 NT-proBNP during 8 to 10 weeks of sacubitril/valsartan were associated with worse outcomes (p = 0.003
296 an, absolute risk reductions with sacubitril/valsartan were more prominent in patients enrolled early
297                     However, candesartan and valsartan were the most potent at blocking AngII-induced
298 th treated HFrEF were switched to sacubitril/valsartan within the first 2 years of Food and Drug Admi
299  the Markov model calculated that sacubitril/valsartan would increase life expectancy at an ICER cons
300 Sensitivity analyses demonstrated sacubitril/valsartan would remain cost-effective vs enalapril.

 
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